ReviewInternational journal of molecular sciences2020
Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Multiple cases of osteopetrosis-like disease in young broiler flocks in Germany.Poultry science · 2026Article
- IGF2BP3 mediates the mRNA upregulation of NLRP3 to promote parathyroid cell proliferation in chronic kidney disease via an m⁶A-dependent manner.Endocrine · 2026Article
- Recurrent Acute Pancreatitis Secondary to Untreated Hyperparathyroidism: A Case Report and Literature Review.Cureus · 2026Article
- Serum-free culture with PVP enables maintenance of primary culture of parathyroid cells in vitro.Bioscience reports · 2026Article
- Pre-Parathyroidectomy PTH as an Integrated Biomarker of Glandular Remodeling and Skeletal Turnover in Secondary Hyperparathyroidism.International journal of molecular sciences · 2026Review
- Parathyroid histology in normocalcemic and hypercalcemic primary hyperparathyroidism with hypercalciuric renal stones.Journal of the Endocrine Society · 2026Article
- Endocrine disorders linked to chronic kidney disease: Mechanisms and clinical implications.World journal of nephrology · 2026Review
- Tertiary hyperparathyroidism with ectopic mediastinal parathyroid adenoma in a patient with chronic kidney disease and cardiovascular complications: a case report.BMC endocrine disorders · 2026Article
- Bone in Parathyroid Diseases Revisited: Evidence From Epidemiological, Surgical and New Drug Outcomes.Endocrine reviews · 2025Review
- Investigation of the association between alterations in mandibular bone structure and serum bone metabolism biomarkers in male patients with chronic kidney disease: a retrospective cohort study.BMC oral health · 2025Article
- [MiR-301a-5p modulates parathyroid hormone secretion in secondary hyperparathyroidism possibly by regulating calcium-sensing receptor].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
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- Assessing causal associations of hyperparathyroidism with blood counts and biochemical indicators: a Mendelian randomization study.Frontiers in endocrinology · 2023Article
- Effect of hemodialysis combined with calcitriol on cardiac function and BNP in patients with hyperparathyroidism secondary to nephropathy.American journal of translational research · 2023Article
- A Molecular Insight of the Role of PIN-1 Promoter Polymorphism (- 667C > T; rs2233679) in Chronic Kidney Disease Patients with Secondary Hyperparathyroidism.Indian journal of clinical biochemistry : IJCB · 2022Article
- Histone Modification on Parathyroid Tumors: A Review of Epigenetics.International journal of molecular sciences · 2022Review
- [Identification of microRNAs targeting vitamin D receptor and their effect on parathyroid hormone secretion in secondary hyperparathyroidism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- [Cultivation and characterization of primary human parathyroid cells from patients with severe secondary hyperparathyroidism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary hyperparathyroidism (SHP) is a common complication of chronic kidney disease (CKD) that correlates with morbidity and mortality in uremic patients. It is characterized by high serum parathyroid hormone (PTH) levels and impaired bone and mineral metabolism. The main mechanisms underlying SHP are increased PTH biosynthesis and secretion as well as increased glandular mass. The mechanisms leading to parathyroid cell proliferation in SHP are not fully understood. Reduced expressions of the receptors for calcium and vitamin D contribute to the disinhibition of parathyroid cell proliferation. Activation of transforming growth factor-α-epidermal growth factor receptor (TGF-α-EGFR), nuclear factor kappa B (NF-kB), and cyclooxygenase 2- prostaglandin E2 (Cox2-PGE2) signaling all correlate with parathyroid cell proliferation, underlining their roles in the development of SHP. In addition, the mammalian target of rapamycin (mTOR) pathway is activated in parathyroid glands of experimental SHP rats. Inhibition of mTOR by rapamycin prevents and corrects the increased parathyroid cell proliferation of SHP. Mice with parathyroid-specific deletion of all miRNAs have a muted increase in serum PTH and fail to increase parathyroid cell proliferation when challenged by CKD, suggesting that miRNA is also necessary for the development of SHP. This review summarizes the current knowledge on the mechanisms of parathyroid cell proliferation in SHP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.